6533b834fe1ef96bd129d842
RESEARCH PRODUCT
Non-adrenergic non-cholinergic nerve-mediated inhibitory control of pigeon oesophageal muscle.
A. PostorinoFileccia RF. BonvissutoS. Abbadessa UrsoT. Vetrisubject
AtropineGuanethidinemedicine.medical_specialtyPotassium ChannelsPhysiologyStimulationTetrodotoxinBiologyInhibitory postsynaptic potentialApaminchemistry.chemical_compoundEsophagusPhysiology (medical)Internal medicinemedicineAnimalsChannel blockerColumbidaeEvoked PotentialsGuanethidineDose-Response Relationship DrugTetraethylammoniumMuscle SmoothNeural InhibitionGeneral MedicineTetraethylammonium CompoundsElectrophysiologyAtropineEndocrinologychemistryApaminPerfusionmedicine.drugdescription
Pigeon oesophageal smooth muscle in vitro has spontaneous electromechanical activity. In the presence of atropine and guanethidine, electrical field stimulation evokes a transient TTX-sensitive response comprising inhibition of electric bursting activity and muscular relaxation. This NANC inhibitory response was analysed using the K+ channel blockers TEA and apamin, TEA perfusion (0.1-5 mM) induced a concentration-dependent reduction in amplitude of EFS-evoked relaxation. Responses to higher stimulation frequencies were more sensitive to TEA than those to lower ones. The maximum reduction in amplitude (29% of control) was obtained on 30 Hz EFS evoked responses during 5 mM TEA perfusion. In a similar way, apamin (0.01-10 microM) perfusion reduced NANC relaxation, up to 30% of control. These results suggest that in the pigeon oesophagus, NANC intramural neurons are responsible for muscular relaxation. We speculate that an increase in K+ conductance might be the main mechanism involved, although the residual response after K+ channel blockade indicates the existence of an additional ionic mechanism.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 1996-01-01 | Archives of physiology and biochemistry |